I am often asked the question “if cannabis was as freely available as alcohol how many would use it and would its harms increase?.  Of course the answer is yes to both. However as about half of young people use cannabis, the increase from removing criminal sanctions would be relatively modest unless it was actively marketed as is alcohol. Certainly the Dutch coffee shop model of regulated but not legalized cannabis access appears not to have increased use since young people in the Netherlands have some of the lowest rates of cannabis use in Europe.

Perhaps the more interesting question is in this circumstance would be what would the net effect on population harms be?  Would liberalising access to cannabis reduce alcohol use to an extent that might reduce the sum total of harms?  This issue is touched on in my new paper in the Journal of Psychopharmacology [Weissenborn and Nutt 2011, Popular intoxicants: what lessons can be learned from the last 40 years of alcohol and cannabis regulation? (PMID:21926420)].  The key points of this paper are briefly outlined below.

A good measure of harm is the costs to the NHS. Hospital admissions for cannabis number less than 1000 per year whereas alcohol now accounts for 1000x as many – over a million last year of which 13,000 were aged under 18yrs.  The role of cannabis in causation of schizophrenia is still controversial – the ACMD in their 3rd cannabis review estimated that to stop one case of schizophrenia one would have to stop 5000 young men or 7000 young women from ever smoking cannabis. Some studies are now suggesting cannabis may help patients with schizophrenia. In contrast, that alcohol causes liver disease is as incontrovertable as is its contribution to the massively accelerating death rates from liver disease in the UK. The frightening contribution that alcohol use makes to domestic violence, child abuse and road traffic accidents were some of the reasons why alcohol scored as the most harmful drug to UK society today in the ISCD scale of drug harms, published in the Lancet last year.

Until the last government induced them to think otherwise by making cannabis a target, the police have always taken the view that cannabis users were much less prone to violence than those intoxicated with alcohol.  Indeed the police were strong supporters of the ACMD recommendation to downgrade cannabis to Class C in 2004. It seems likely that the recent rise in alcohol intake in the UK may have been in part due to the pressure of anti-cannabis policing leading to young people switching their preferred intoxicant to alcohol.

Estimating the true relative harms of alcohol and cannabis is not easy as there are no societies today where the two drugs are equally available. However where neither are legal – as in some Islamic states – alcohol appears to cause more dependence than cannabis, even in Morocco a traditional cannabis growing country.

Taken together we estimate that alcohol is at least twice as harmful to users than cannabis and 5 times more harmful to society. The obvious conclusion is that the current legislation criminalising cannabis users is illogical as well as inhumane and may be causing much more harm than it does good. Time for a rational intervention Mr Cameron?

The full paper can be found in the Journal of Psychopharmacology http://jop.sagepub.com/content/early/2011/09/03/0269881111414751

A guest post by Dr Les King.

The control of mephedrone and related compounds under the Misuse of Drugs Act in April 2010 was largely prompted by the media attention given to numerous alleged mephedrone fatalities. Subsequent toxicology examinations showed that most of those deaths were not caused by mephedrone, a finding now underscored by the latest statistics (REF 1) from the Office for National Statistics (ONS). In 2010, in England and Wales, there were just 6 deaths where mephedrone was mentioned on the death certificate. By comparison, there were 144 fatalities where cocaine was mentioned. The significance of this comparison can be understood when it is recognised that cocaine is a drug which was often substituted by mephedrone. The number of deaths alone does not tell us much about the intrinsic toxicity of a substance. However, the ratio of the number of deaths to suitable proxy measures of prevalence does provide a useful index (REF 2). The British Crime Survey (Drug Misuse Declared) (REF 3) provides one such denominator. For 2010/2011, it was reported that in England and Wales, 4.4% of 16 to 24 year olds used mephedrone in the last year. This was the same as the number using cocaine, a figure only increased to 4.7% if crack cocaine is also included. If we choose instead to look at last year use by 16 to 59 year olds, the respective proportions were: mephedrone = 1.4% and cocaine = 2.1%. Caution may be needed in interpreting the small number of mephedrone deaths in 2010, and it is possible that some cases were missed because not all toxicology laboratories were able to identify this new substance. The mortality statistics also suffer from other confounding issues, as discussed by Bird (REF 4), but it would seem that regardless of which age group we consider, and bearing in mind the uncertainties, the fatal toxicity of mephedrone is low by any standard, and may be less than 10% of that of cocaine. This confirms the concerns raised by Bird (REF 5); an unintended consequence of banning mephedrone would be a lost opportunity to save the lives of many who would succumb to cocaine poisoning.

1. Deaths related to drug poisoning in England and Wales, 2010. Office for National Statistics, 23 August 2011
2. L.A.King and J.M.Corkery, 2010, An index of fatal toxicity for drugs of misuse, Hum. Psychopharmacol. Clin. Exptl., 25, 162-166
3. Drug Misuse Declared: Findings from the 2010/11 British Crime Survey, England and Wales, Home Office, 28 July 2011
4. S.Bird, 2011, Drugs deaths in England and Wales – a wake-up call to the Registrar General, http://www.straightstatistics.org/article/drugs-deaths-england-and-wales-wake-call-registrar-general
5. S.Bird, 2010, Banned drug may have saved lives, not cost them, http://www.straightstatistics.org/article/banned-drug-may-have-saved-lives-not-cost-them

For 30 years we have had a systematic attack on the safety of ecstasy [MDMA]. This has been fueled by a desire by governments, lobbyists and some scientists to justify the illegal status of this drug which in the UK is at the very highest level – Class A. This puts it alongside drugs such as crack cocaine and heroin which by all scientific assessments are much more harmful [Nutt King and Phillips 2010].

Much of the so called scientific evidence that has been used to justify MDMA as being harmful is flawed, some just simply wrong as they used the wrong drug [Ricaurte et al 2002] and most findings are exaggerated. For example, a well reported recent study that claimed to provide proof that MDMA impaired memory in fact found a minimal effect in only one memory measure that was of no clinical significance. This was taken as proof that MDMA damaged the brain despite the fact that on some other measures of brain function, the MDMA-using group performed better than the controls [Schilt et al 2007].

It appears there is an assumption that MDMA will damage human brains because in studies in some animal species [rats and monkeys] it can lead to damage to the serotonin nerve cells. These effects are most pronounced at high doses and are not seen when human equivalent doses are used [Fantegrossi et al 2004]. But still the concern is there, at least in the mind of the Home Sec Jaqui Smith when she announced that MDMA would remain Class A against the recommendations of the ACMD. She said that as long as there were “public concerns” about the risks of ecstasy on the brain she would not be moved, even though these concerns were largely manufactured by the media and magnified by bad science on ecstasy [Forsyth 2001].

However you might feel that as all drugs may be harmful then ecstasy could surely only be harmful also?  Well maybe not. We should remember that MDMA was developed as a therapeutic tool for psychotherapy and its successful role here was severely curtailed when the drug was made illegal. Thirty years on, MDMA has only recently been reintroduced into clinical trials with great success in one study in resistant PTSD [Mithoefer et al 2010].

But what about the rats – does it still cause brain damage there? A new paper shows an intriguing effect and one, which many will find paradoxical: MDMA improved recovery from brain injury rather than worsening it [Edut et al 2011]. This paper has not apparently received any media attention so far which I why I felt compelled to do what I could to make it more widely known.

However the results are not so paradoxical if one remembers that the potential utility of such stimulant drugs to aid recovery from brain trauma was first reported over 30 years ago for amfetamine [see Gladstone and Black 2000]. I have made efforts to get stimulant drugs tested in clinical trials for the brain injured in the UK but always their controlled status makes using them difficult. Doctors are frightened, ethics committees worried, special licenses are required and are expensive and patients and relatives concerned (if it’s classified then it must be surely be dangerous?). For these reasons, we need to work to minimise the damage that legal controls on drugs have to impede research. The recent banning of mephedrone and naphyrone is likely to significantly limit new drug discovery in the area of antidepressants and anti-addiction agents [Nutt 2010, Nutt 2011].

Lets hope that this intriguing new finding of the potential therapeutic benefit of MDMA as a brain repair agent is taken up by the medical and scientific communities working in the fields of stroke and brain trauma. Some encouragement from the media could help this process.


Edut S, Rubovitch V, Schreiber S, Pick CG (2011) The intriguing effects of ecstasy (MDMA) on cognitive function in mice subjected to a minimal traumatic brain injury (mTBI)  Psychopharmacology 214, Number 4214, 877-889, DOI: 10.1007/s00213-010-2098-y

Fantegrossi WE, Woolverton WL, Kilbourn M et al. (2004) Behavioral and neurochemical consequences of long-term intravenous self-administration of MDMA and its enantiomers by rhesus monkeys. Neuropsychopharmacology 29(7): 1270–81.

Forsyth A Distorted? a quantitative exploration of drug fatality reports in the popular press International Journal of Drug Policy 12 (2001) 435–453

Gladstone DJ, Black SE. Enhancing recovery after stroke with noradrenergic pharmacotherapy: a new frontier? Can J Neurol Sci. 2000 May;27(2):97-105

Mithoefer et al (2010) The safety and efficacy of _3,4-methylenedioxymethamphetamineassisted psychotherapy in subjects with chronic, treatment-resistant posttraumatic stress disorder: the first randomized controlled pilot study. Journal of Psychopharmacology. July 2010.

Nutt 2010

You say precaution, I say perversion: eight harms deriving from the precautionary principle


The ACMD and naphyrone – another example of evidence-free policy making?

Nutt 2011 Perverse effects of the precautionary principle: how banning mephedrone has unexpected implications for pharmaceutical discovery Therapeutic Advances in Psychopharmacology Editorial – in press

Nutt DJ  King LA Phillips LD (2010) Drug harms in the UK: a multicriteria decision analysis  Lancet 376: 155866

Ricaurte GA, Yuan J, Hatzidimitriou G et al. (2002) Severe dopaminergic neurotoxicity in primates after a common recreational dose regimen of MDMA (“ecstasy”). Science 297: 2260–3. Retraction printed in: Science (2003) 301: 1479.

Schilt T, Maartje ML de Win, Koeter M et al. (2007) Cognition in novice ecstasy users with minimal exposure to other drugs. Archives of General Psychiatry 64: 728–36.

Blair’s Other War

April 26, 2011

I write this from Mexico, where the ‘War on Drugs’ and clashing drug cartels have claimed thousands of lives. The billions of dollars worth of aid being pumped in countries in South America, Afghanistan and elsewhere have resulted in, at best, the ‘balloon effect’, where production is pushed down in one area only to pop up in another. In the fifty years since the 1961 UN Single Convention on Narcotic Drugs, the ‘War on Drugs’ has morphed from a figurative battle to a literal one. The fog of war has driven politicians to go beyond the bounds of law in their lust for battle: the Single Convention allows for the medical and scientific use of controlled drugs and yet, many countries interpret it as prohibiting all use of all Schedule I drugs, hindering potentially life changing research.

Domestic law has also been trampled upon in the rush to act tough on drugs. The UK’s 1971 Misuse of Drugs Act [MDAct] was designed to remove decision-making about drugs from the party politics of parliament to minimise the risk that short term party interests might lead to bad laws.  The MDAct classified drugs in three levels – A B C – based on their relative harms of drugs, which were decided upon by an expert group, the ACMD [Advisory Council on the Misuse of Drugs]. This worked well for the first 30 years and even Margaret Thatcher accepted its recommendations on needle-exchange to limit HIV spread.  Though this went against her political philosophy, she accepted that it was logical to be guided by experts and was rewarded by the UK leading the world in terms of slowing the rate of HIV spread from intravenous drug use.

In the last decade under Tony Blair’s government, things began to change. It decided it knew better than experts and hunted for evidence to support its policy decisions rather than the other way round.  In late 2004, Blair decided to wage a different type of war – this time on drugs. For unknown reasons – at least not explained in his autobiography – he decided to ignore the MDAct (i.e. break the law)  and make decisions on drugs without consulting the experts on ACMD. He convened a special meeting of senior police, military and customs officials, from which the war was initiated.

The first salvo was aimed at magic mushrooms. These were legal at the time  but the government decided that they had to be hard on head-shops selling freeze-dried preparations so they made them a Class A drug without consulting the ACMD.  The well known adage  “the first casualty of war is the truth” certainly applied to the mushroom decision as by no metric are mushrooms as harmful as the real Class A drugs such as crack cocaine and heroin.

The mushrooms were an easy battle to win and perhaps this rewarding feeling of success fueled the next campaign against cannabis. In 2004, all preparations of cannabis had been made Class C (they had been either Class A or Class B previously). This downgrading was made after an extensive review of the evidence by the ACMD, yet was viciously opposed by parts of the media and many politicians.  From that date a concerted war was waged against cannabis users justified by statements that cannabis, particularly the new variant skunk, was more harmful than its Class C status would indicate.

Gordon Brown continued the war when he took over as Prime Minister. Within weeks of coming to power, he made the absurd claim that “skunk was lethal” when in reality cannabis, in contrast to alcohol and controlled drugs, has never killed anyone by direct toxicity/poisoning.  He oversaw  a new Home Office war policy of increasing convictions for cannabis users in an attempt to deter use. This doubled the number of people convicted for cannabis possession from 88,000 in 2004/5 to 158,000 in 2007/8.  Police with sniffer dogs became a common site on London tube stations where young men were searched and prosecuted if cannabis was found.  That this behaviour almost certainly breached their human rights was ignored; rights have a lesser place when at war. Predictably an even greater injustice was seen by the ethnic bias in convictions with Asian and Afro-Caribbean men being significantly overrepresented.

Worse, the war extended to those using cannabis for medicinal purposes such a people with multiple sclerosis or spasticity. Police would conduct dawn raids on possible users, smashing down their front doors just in case they might leap from their wheelchairs and abseil out the window! Why? Because violence is what wars allow, if not demand.

The war on medicinal cannabis became more aggressive in 2005 when the Law Lords seriously aggravated the situation of those using cannabis for medicinal purposes. They colluded with the government by changing the law to disallow the centuries old “Defense of Necessity” for medicinal cannabis use. This common law allows users to plead that their use of a drug was simply and solely to ameliorate a medical condition for which other treatments had not worked.  The Law Lords decided that since the government had decreed that cannabis was sufficiently harmful to be a Class B drug, patients should be deterred from using it by removing this defense. A truly cruel and inhumane piece of legislation that brings shame on those who enacted it and great distress to those prosecuted because of it.  However it was predictable as the corruption of the law is a recognized element of war.

The final battle before my sacking was on MDMA (ecstasy). This had been classified alongside cocaine and heroin as a Class A drug ever since it was made illegal. This was patently absurd from any evidence-based perspective but the government had actively resisted any attempts to review the evidence on which ecstasy was classified until ordered to do so by a Select Committee report. When the ACMD with the help of a NICE health technology assessment unit reported that its harms had been overestimated and were commensurate with a Class B status, the government refused to reclassify.

My response to both the cannabis and ecstasy decisions was to point out how they undermined the scientific integrity of the MDAct and, by allowing longer than appropriate prison sentences, were bound to lead to injustice. Moreover, I believed that these decisions could increase the harms from legal drugs particularly alcohol; by scaring people from ecstasy and cannabis they might be increasing use of alcohol, a more harmful drug.  By fighting battles on mushrooms, cannabis and ecstasy the government was deflecting attention away from the rising tide of deaths from alcohol.

Military wars are evaluated through public enquiries – surely it is time to seek the truth about the war on drugs and make good the damage done to drug users, their families and the scientific process caused by this unhappy example of political lust for wars.

In this guest post, Dr Les King and Rudi Fortson Q.C.  highlight how the last government’s meddling in legislation regarding cathinones, including mephedrone, at this time last year has generated confusion for forensic scientists and legal practitioners regarding the precise placing of some cathinones within Class B.  It is a problem that is only now being addressed.

Instead of accepting the generic definitions of cathinones drafted by members of the ACMD that would cover all the various types of cathinones, the Home Office took the unusual step of changing the legislation to specifically mention mephedrone to ‘send a message’ to the public, presumably in response to the (unfounded) hysteria over mephedrone use by young people.  In taking this course, one variant of methylmethcathinone (mephedrone) was listed in one sub-paragraph of Part 2 of Schedule 2 to the MDA, while other variants of methylmethcathinone were listed in another sub-paragraph, thereby generating confusion.  Logically, all variants of that substance ought to have been classified as a single group.     To understand  how this came about requires a little more understanding of the chemistry of cathinones.

Dr King explains: The crux of the problem is peculiarly technical, but rests on the existence of mephedrone isomers. While mephedrone is 4-methylmethcathinone , both 2- and 3-methylmethcathinone  can also exist. To distinguish those different isomers is a challenging task for a laboratory, and certainly cannot be done by the routine methods used in drug analysis. That is where well-crafted generic control is so useful: all three isomers can be controlled without ever mentioning them by name in the Act or needing to be analytically-specific about which one has been found in a questioned sample.

That advantage was lost following Home Office tinkering. Eventually, following many discussions between the forensic science community and the CPS, a legally acceptable work-around was concocted. Yet that legal fudge could only be a temporary measure, which is why the Government has announced that the original clauses in the Modification Order of 2010 will now be replaced with what should have been there in the first place. This is a clear case of government acting without a clear understanding of the issues. Instead of supposedly protecting the public from harm with the controlling of mephedrone, the previous government unnecessarily weakened legislation for political gain.
However, whilst recognising the advantages of generic descriptions from a technical point of view, Rudi Fortson has expressed a note of caution.  For him, the law should not only be precise but it should also be clear and capable of being understood by lawyers and non-lawyers alike.  There is a risk that various substances, readily identifiable by their popular name (such as “mephedrone”), will be lost in the language of chemistry, making it difficult for non-chemists to identify, when reading the MDA, which drugs are controlled and which are not.



Addiction is a major health problem that costs as much as all other mental illnesses combined (about £40 billion per year) and about as much as cancer and cardiovascular disorders also.

At its core addiction is a state of altered brain function that leads to fundamental changes in behavior that are manifest by repeated use of alcohol or other drugs or engaging in activities such as gambling.  These are usually resisted, albeit unsuccessfully, by the addict.  The key features of addiction is therefore a state of habitual behaviour such as drug taking or gambling that is initially enjoyable but which eventually becomes self-sustaining or habitual. The urge to engage in the behaviour becomes so powerful that it interferes with normal life often to the point of overtaking work, personal relationships and family activities. At this point the person can be said to be addicted: the addict’s every thought and action is directed to their addiction and everything else suffers. 

If the addictive behaviour is not possible e.g. because they don’t have enough money then feelings of intense distress emerge. These can lead to dangerously impulsive and sometimes aggressive actions.  In the case of drug/alcohol addiction the situation is compounded by the occurrence of withdrawal reactions which cause further distress and motivate desperate attempts to find more of the addictive agent. This urge to get the drug may be so overpowering that addicts will commit seemingly random crimes to get the resources to buy more drug. It has been estimated that about 70% of all acquisitive crime is associated with drug and alcohol use.

Addiction is driven by a complex set of internal and external factors.  The external factors are well understood:  the more access to the desired drug or behaviour e.g. gambling the more addiction there is. 

The internal factors are less clear. Although most addiction is to alcohol and other drugs, addiction to gambling and other behaviours such as sex or shopping can occur. These tell us that the brain can develop hard-to-control urges independent of changing its chemistry with drugs.  All addictions share a common thread in that they are initially pleasurable activities, often extremely enjoyable. This results in these behaviours hijacking the brain’s normal pleasure systems so that naturally enjoyable activities such as family life, work, exercise become devalued and the more excessive addiction behaviours take over. 

However, not everyone who engages in drug use or gambling becomes addicted to them so clearly other factors are important. These are not yet understood but are now being actively studied. Some people may be particularly sensitive to the pleasurable effects of alcohol, drugs or gambling, perhaps because of coming from deprived backgrounds. In others, addiction may occur because of an inability to adopt coping strategies.  Others may have an underlying predisposition to develop compulsive behaviour patterns. Some unfortunate people may have several of these vulnerability factors and there are also genetic predispositions to some of them.

Also a significant amount of drug use is for self-medication, examples include  cannabis for insomnia, alcohol to reduce anxiety, opioids for pain control etc. This therapeutic use can escalate into addiction in some people though by no means all. Not all drugs which are used for recreational purposes are addictive. LSD and magic mushrooms seem not addictive at all, and some have a low risk of addiction (MDMA/ecstasy; cannabis). The most addictive drugs are nicotine, heroin and crack cocaine plus metamfetamine (crystal meth) although this is not much used in the UK.

Just because some people – including leading politicians – have used drugs but stopped before they became addicted does not mean that anyone can stop that easily.  Starting to use drugs may be a lifestyle choice but once addiction sets in, choosing to stop is very much more difficult if not impossible.

We are beginning to understand how addictions start in the brain. The pleasurable or rewarding effects of addictions are mediated in the brain through the release of chemicals such as dopamine [by cocaine, amphetamines, nicotine] or endorphins [heroin] or both [alcohol].  The pleasures are then laid down as deep-seated memories, probably through changes in other neurotransmitters such as glutamate and GABA that make memories. These memories link the location, persons and experiences of the addiction with the emotional effects. These memories are often the most powerfully positive ones the person may ever experience, which explains why addicts put so much effort into getting them again.  When the memories re-occur, which is common when people are still using drugs or gambling, as well as when in recovery/abstinence, they are experienced as cravings.  These can be so strong and urgent that they lead to relapse.

A great deal of research has been conducted into the role of dopamine in addiction and we now know that the number of dopamine receptors seems to predispose to excessive pleasure responses from stimulant use. This excessive response is thought to initially occur in the reward centre of the brain – [the nucleus accumbens] – but then move into other areas where habits are laid down.  This shift from voluntary (choice use) to involuntary (habit-use) explains a common complaint of addicts that they don’t want to continue with their addictions, and even that they don’t enjoy them anymore, but cant stop themselves.  In this sense addiction can be seen as a loss-of-control over what starts out as a voluntary behavior.  Thus addiction is not, as some like to suggest, simply a “lifestyle” choice. It is a serious, often lethal, disease caused by an enduring (probably permanent) change in brain function.

We know that personality traits especially impulsivity, predict excess stimulant use and in animals this can be shown to correlate with low dopamine and high opioid receptor levels.  Similarly in humans low dopamine and high opioid receptor levels in brain predict drug use and craving.  These observations give new approaches to treatment, both psychological interventions such as behavioural control, and anti-impulse drugs such as those used for ADHD e.g. atomoxetine and modafinil, are being tested. 

For some addictions, especially heroin, the risk to the addict (life expectancy less than that from many cancers) and to society (from crime and infections), is so high that the prescription of substitute opioid drugs or even heroin itself saves lives and reduces crime. These substitute drugs are methadone and buprenorphine [Subutex]. As well as reducing crime and social costs by removing the need for addicts to commit offences to feed their habit, they also protect from accidental overdose and reduce risk of infections such as HIV and hepatitis.  Similar substitute pharmacological approaches exist for other addictions e.g. gammahydroxybutyrate (Alcover) and baclofen for alcohol addiction, and varenicline (Champix) for nicotine dependence.

Another major reason for relapse in addiction is stress. This may work through increasing dopamine release in brain so priming this addiction pathway or by interactions with other neurotransmitters such as the peptide substance P. As antagonists of these neurotransmitters are now available they are being tested in human addictions and may offer an alternative to substitution treatments.
Further reading

Nutt DJ  King LA Phillips LD (2010) Drug harms in the UK: a multicriteria decision analysis  Lancet 376: 1558-66

Nutt DJ Lingford-Hughes A (2008) Addiction the clinical interface Brit J Pharmacology 1-9

Nutt DJ, Law FD (2008) Pharmacological and Psychological aspects of drug abuse. New Oxford Textbook of Psychiatry 2nd edition

Robbins TR, Everitt B,  Nutt DJ (2010) The Neurobiology of Addiction – New Vistas.   OUP

A guest blog from Paul Myles

Alcohol is a major public health problem and one that is growing in young people mostly from the increase in binge drinking. There are several reasons for the increase in drinking in this age group particularly the availability of low priced strong ciders lagers and breezers but advertising plays a significant role as well.

The recent BMA publication ‘Under the Influence’ [British Medical Association 2009] clearly shows that the drinks industry cynically targets very young people, revealing the techniques that they employ, of which many parents are unaware.  These include targeted email campaigns with embedded film clips advertising alcohol, Facebook links and mobile phone text messaging.

How can we combat this sophisticated and cynical approach? One approach is to tell young people directly of the dangers of alcohol. However it seems that direct scare tactics about the outcome of alcohol use or any other substance that can be misused has been ineffective and may even be counterproductive (Drugscope 2010) (Coggans et al 1991).

Another way is to develop a teaching module for school students that reveals the subtle ways in which positive messages about alcohol are communicated. This how now been done and piloted in East Sussex with great success.

The teaching module shows the students how the drinks industry makes its own voluntary codes and them blatantly ignores them. It shows how the Portman Group [that has responsibility for alcohol education] whilst appearing to be concerned about alcohol harm is actually dominated by the drinks industry. Also it is revealed that the public health message in the UK  is left to the drinks industry. The myths surrounding alcohol are discussed and then the students are asked to make up their own mind about the issues. Profit motives of the drinks industry, the tax income and political agendas are exposed and compared with the cost to society, mortality and shortening of life caused by alcohol use.

The rationale for the module is to enable students to critically evaluate the way that young people are targeted to buy alcohol. The lessons examine the mechanics behind the commercial enterprise of alcohol sales. The students analyse the management /mismanagement of the substance misuse issue.

This approach does what the advertisers do, get this message out to as many people as possible, to show the public how they are being hoodwinked by the drinks industry. It is hoped that the British public will realise that they are being duped and react accordingly by contacting their MP and local authorities.

The Independent Scientific Committee on Drugs (ISCD) is now working to see how this might roll out the programme to many more schools


This comprehensive package includes a 2 lesson module for students, a teacher training session and a presentation to parents and interested members of the community developed by Paul Myles from his MSc research at Sussex University. The module contains multi media and is designed to address a wide spectrum of learning abilities. The lesson plans were developed by researcher Paul Myles supported by East Sussex County Council.

British Medical Association 2009. Under The Influence:The damaging effect of alcohol marketing on young people. BMA Science and Education Department and the Board of Science. BMA Marketing & Publications London. www.bma.org.uk

Coggans N, Shewan D, Henderson M and Davies JB ‘National Evaluation of Drug Education in Scotland’, ISDD 1991.

Paul Myles BSc Psychol (Hons) MSc Substance Misuse MBPsS

Paul is a Fellow of the Royal Society of Medicine and a Graduate member of the British Psychological Society contact 01273 477723 pmyles@btclick.com 13 Hill Rd Lewes Sx BN7 1DB